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COPPER DEFICIENCY IN THE RAT
Author(s) -
Gallagher CH,
Reeve Vivienne E,
Wright R
Publication year - 1975
Publication title -
australian journal of experimental biology and medical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0004-945X
DOI - 10.1038/icb.1975.39
Subject(s) - cytochrome c oxidase , mitochondrion , copper deficiency , oxidase test , biochemistry , toxicity , adenine nucleotide , endocrinology , catabolism , medicine , nucleotide , chemistry , biology , metabolism , enzyme , copper , organic chemistry , gene
Summary Daily administration of increasing closes intraperitoneally of 2·5–4·0 mg NaCN/kg to male Wistar rats for 5 weeks produced acute signs of poisoning immediately post‐injection hut no sign of chronic toxicity except lower final body weights than in control rats. CN − ‐treated rats had less liver copper than controls, but not below the range of normality, and their liver mitochondrial membranes were 24% less able to bind adenine nucleotides than control membranes. No other biochemical or pathological sign of copper deficiency occurred. Liver cytochrome oxidase activity was normal after the 5 weeks of CN − administration, as was the ability of liver mitochondria to synthesize phospholipids. The ultrastructure of hepatocytes was normal without evidence of the enlarged, misshapen mitochondria produced by copper deficiency. Normal cytochrome oxidase activity of liver mitochondria, together with reduced liver copper levels and reduced binding affinity of mitochondrial membranes for adenine nucleotides, indicate that the membrane binding site for adenine nucleotides is not cytochrome oxidase per se but may involve copper, perhaps by virtue of its cationicity. With repeated exposure to CN − rats develop tolerance to acute poisoning. It is suggested that this may he due to the switch in glucose cata‐bolism towards the pentose pathway at the expense of other pathways.